Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 125, Issue 6, Pages 2220-2227Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI78087
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Funding
- NIH [K01AR060781, R01AI42269, R37AI49954, R01AI068787, R01AI085567, R01AR064350]
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Systemic lupus erythematosus (SLE) is a prototype systemic autoimmune disease that results from a break in immune tolerance to self-antigens, leading to multi-organ destruction. Autoantibody deposition and inflammatory cell infiltration in target organs such as kidneys and-brain lead to complications of this disease. Dysregulation of cellular and-humoral immune response elements, along with organ-defined molecular aberrations, form the basis of SLE pathogenesis. Aberrant T lymphocyte activation due to signaling abnormalities, linked to defective gene transcription and altered cytokine production, are important contributors to SLE pathophysiology. A better understanding of signaling and gene regulation defects in SLE T cells will lead to the identification of specific novel molecular targets and predictive biomarkers for therapy.
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